A patient with metastatic melanoma initially responded after adoptive T-cell transfer, but an inflammation-induced melanoma cell dedifferentiation resulted in loss of the MART1 tumor antigen and tumor relapse.

Deletions of the mono-ADP-ribosylhydrolase gene MACROD2 enhance intestinal tumorigenesis in a haploinsufficient manner by suppressing PARP1 activity, leading to increased sensitivity to DNA damage and driving chromosome instability.

Melanoma tumorigenesis is accelerated by the uptake of long-chain fatty acids from adipocytes via the FATP1 lipid transporter, and this adipocyte-melanoma cell cross-talk may by disrupted by FATP inhibitors.